It is well appreciated however that top level sportsmay sometimes overtax the body, and can lead to injuries, most notably of a musculo-skeletal nature. The lecture today, by Prof. Hein Heidbuchel, University of Leuven, defends the thesis that the heart also can develop sports injuries.
The heart adapts to sports in a marvellous fashion, in what is generally described as “athlete’s heart”. This mainly consists of a balanced hypertrophy and/or dilatation of the four heart chambers. These changes by themselves however may have a pro-arrhythmic potential, both on a supraventricular and on a ventricular level.
Not only can arrhythmias be influenced by changes in autonomic tone, like vagotonia at rest and a highly catecholaminergic state during exertion, also, dilation and hypertrophy of the atria in an athlete's heart may facilitate development of atrial fibrillation. More and more evidence has emerged over the last decade linking frequent vigorous sports activity (often endurance) to atrial flutter and fibrillation.
It is also recognised that the sinus bradycardia which is the hallmark feature of athlete's heart is not only due to increased vagotonia, but also to an intrinsic slowing of the heart rate. This inherent bradycardia may not be fully reversible and has been linked with a slightly increased risk for sinus node disease and even the need for pacemaker implantation later in life.
Ventricular arrhythmias are rare in athletes, but these arrhythmias may be life-threatening of course. Physical activity is associated by a 2.8 times increased risk for sudden death. The classical concept is that arrhythmic events are due to an underlying (structural or electrical) heart disease, on which physical activity acts as a trigger for initiation of arrhythmias.
The thesis presented by Prof. Heidbuchel adds a second (additional) hypothesis, which he introduced in 2003: intense endurance activities will put a particularly high strain on the right ventricle which may be harmful in some. Excessive RV strain may lead to minor cell damage after an endurance event, as evidenced by cardiac enzyme elevations. Over time, repetitive injury may lead to changes that resemble right or (less often) left ventricular cardiomyopathy, even in the absence of underlying demonstrable genetic abnormalities.
The syndrome of 'acquired arrhythmogenic RV cardiomyopathy' is rare, although it may easily be overlooked. Sports cardiologists, like orthopaedics, should be prepared to realise that excessive sports activity can lead to cardiac sports injuries in some, which will help to counsel on safe participation in all.
Vexing issues in sports cardiology, 11:30 – 13:00, Room 2, 16 April 2011
